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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Air embolism, diagnosed by clinical therapeutic trial in the Navy hyperbaric chamber, occurred in a woman having labor induced by hypertonic saline for intrauterine fetal death at 25 weeks' gestation. 20 hours after saline administration, and 2 hours after 2 mU/minute diluted oxytocin was started, she had a sudden cardiovascular collapse with cyanosis and dyspnea. She was resuscitated by ventilation by mask and iv fluids. When she regained consciousness she was cortically blind. During treatment by the Navy's protocol, 30 minutes of compression at 6 ATA alternating cycles of 100% oxygen and air after rapid decompression to 2.8 ATA for 5 hours 19 minutes, there was a dramatic improvement in vision. After treatment, she showed left hemianopsia with macular damage. A year later only slight loss of left visual field remained. Air embolism can only be differentiated from amniotic fluid embolism by demonstration of amniotic fluid or fetal components in the maternal central circulation, or a therapeutic trial in a hyperbaric chamber. It is safer to try the pressure chamber immediately.
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PMID:Air embolism following intra-uterine hypertonic saline instillation: treatment in a high-pressure chamber; a case report. 259 57

A case of severe vasoconstriction treated as cardiorespiratory collapse in a woman given extraamniotic PGF2alpha for midtrimester abortion is described, with comments on management of this rare reaction. The patient was having elective termination because of confirmed spina bifida with hydrocephalus by ultrasound and elevated AFP at 18 weeks gestation. She was given a 4 mg test dose of PGF2alpha (Dinoprost, Upjohn Pty, Ltd) in viscous gel (Tylose MH300, Hoechst Australia Ltd) via extraamniotic Foley catheter. She immediately developed dyspnea, abdominal and breast pain, hypotension of 50 mm Hg systolic, peripheral vasoconstriction, cyanosis and confusion. She was treated with iv Hartmann's solution 600 ml, oxygen 8 1/min, and sc adrenaline 1/1000 0.5 ml. She seemed to improve after receiving 500 ml 3.5% polygeline colloid (Haemaccel, Behringwerke AG), and 5 ml 1/10,000 adrenaline iv, as her systolic blood pressure rose to 70 mm Hg measured indirectly. 500 ml more iv colloid was given, and blood pressure rose to 90 mm Hg. Then she suddenly deteriorated with florid pulmonary edema. Oxygen saturation fell and positive pressure ventilation was begun. She was given furosemide 160 mg iv and hydrocortisone 500 mg iv. Anaphylactic reaction was ruled out on the basis of blood count; amniotic fluid embolism was ruled out because of minor changes in clotting parameters. The events seen here most likely occurred as a result of inadvertent injection of PGF2alpha into the arterial circulation, causing increased pulmonary arterial pressure and vascular resistance, systemic vasoconstriction interpreted as hypotension, all exacerbated by adrenaline and exogenous fluid load. Severe hypertension after extraamniotic PGF2alpha has been reported before in a similar case of apparent hypotension treated with agents to increase blood pressure. PGF2a should not be used without facilities to treat such adverse reactions.
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PMID:Cardiorespiratory collapse and pulmonary oedema due to intravascular absorption of prostaglandin F2 alpha administered extraamniotically for midtrimester termination of pregnancy. 260 61

Spontaneous rupture of the esophagus (Boerhaave's syndrome) usually presents in a dramatic fashion. Classically, following repeated episodes of vomiting, patients present with chest pain, dyspnea, cyanosis, shock, and cardiovascular collapse. We present a case of occult Boerhaave's syndrome diagnosed by an upper gastrointestinal series in a 33-year-old man who arrived at the emergency department with a chief complaint of hematemesis. This case report reviews the usual presenting signs and symptoms of Boerhaave's syndrome and concludes with a caution to physicians not to ignore the possibility of this disease entity in relatively stable patients.
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PMID:"Occult" Boerhaave's syndrome. 328 11

This paper discusses causes, hemodynamics, symptoms, and signs of pulmonary embolism. Severe cases obstruct at least 60 percent of the pulmonary vascular bed. Small or moderate cases may be easily overlooked. Symptoms may be only slight chest pain or dyspnoea, fever, giddiness, or irregular heart beat. In the author's experience with 35 cases of acute massive pulmonary embolism at the Bromptom Hospital oral contraceptives were considered a predisposing factor in 5 cases (14 percent), pregnancy was a possible cause in 2 (6 percent), a recent operation in 24 (68 percent). No other recognized factor was thought to have predisposed more than a single case. Clinical features included cyanosis, collapse, sever chest pain, dyspnoea, sweating, rapid heart rate, falling blood pressure, and occasional coughing up of blood. Electrocardiograms sometimes gave helpful information. Chest x-ray was usually not helpful except to exclude other causes. Heart catheterization and pulmonary arteriography have been done to assess the extent of the embolism. Emergency surgical pulmonary embolectomy is recommended for extreme cases. Fibrinolytic agents such as streptokinase may be adequate for less severe cases who have not had a recent operation of do not suffer from a hemorrhagic disorder.
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PMID:Pulmonary embolism. 535 32

127 cases of tracheal dyskinesia were seen in infants and children out of which 87 were 1 to 12 months of age. The diagnosis was based on the existence of a collapse reducing the tracheal diameter of more than 50% on endoscopy. Endoscopic examination was performed without general anesthesia. This material represents 5,8% of the patients submitted to this procedure. 85 patients had "primitive" dyskinesia and 42 had major associated abnormalities. Uni or bilateral bronchial dyskinesia was associated in 43% of the cases. The four commonest presenting symptoms were a stridulous or wheezing respiration, recurrent bronchitis, chronic cough, cyanosis. The frequency of associated digestive troubles: gastroesophageal reflux aspiration was noteworthy. Several functional consequences were encountered: hypoxemia, hypercapnia, abnormalities of FRC, increased RL, lowering of dynamic compliance, alterations of perfusion and ventilation on scintiscans. The prognosis was good in primitive cases. Two deaths occurred, in the group with associated abnormalities. The pattern of the patient with primitive dyskinesia and that of the patient with dyskinesia and associated abnormalities are outlined. Some features remarkable in this series of patients are pointed out in a discussion of the pathophysiology of the syndrome. Increased transmural pressure is not a common cause of tracheal dyskinesia and infection as well. The possibility of a temporary intrinsic anomaly of the tracheal wall is suggested. Even if its exact mechanism remains unknown, tracheal dyskinesia is a distinct entity observed in infants and children. It appears as a common cause of recurrent bronchopulmonary disease in the young.
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PMID:[Tracheal dyskinesia (tracheomalacia) in infants and children. Study of 127 cases diagnosed through endoscopic examination (author's transl)]. 626 18

Tracheomalacia is a rare congenital malformation of the tracheobronchial cartilages in which the supporting cartilaginous rings permit expiratory collapse of the airway. The condition is usually mild and self-limited. There is a severe variant, however, that is life-threatening and warrants separate categorization. Four children with severe primary tracheomalacia were treated recently. The clinical symptoms, diagnostic findings, and eventual treatment of these patients were highly distinctive and almost identical in all 4, permitting us to make the following observations: (1) primary severe tracheomalacia must be suspected in infants with unexplained respiratory distress manifested by stridor and cyanosis; (2) symptoms are not present at birth but appear insidiously after the first weeks of life, are markedly aggravated by respiratory tract infections, and are made worse by agitation; (3) bronchoscopy is essential for definitive diagnosis and should be employed early in the diagnostic process; (4) tracheostomy is probably essential in most instances; and (5) resolution, although spontaneous, does not occur until after 2 years of age.
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PMID:Primary tracheomalacia. 684 90

This is case history of a primigravid woman on whom Caesarean section was carried out in normal conditions for fetal distress, the patient being placed in Trendelenburg position. After the abdomen had been closed there was a sudden collapse with cyanosis, right bundle branch block and then coma with hypertonicity, hyperreflexia and transitory hemiplegia. The only possible diagnosis that could be made was of air embolus following Caesarean section in the light of many investigations that were carried out and the improvement under hyperbaric oxygen treatment and the very irregular progress of the neurological symptoms. Published case histories are rare [12] (published by Walrop, 1953 and Nelson 1960) and over all the result has been unfavourable. The diagnosis can be proven when gas has been found in the blood vessels at autopsy or by the finding of certain clinical signs which indicate the presence of air in the heart or in the blood vessels (water mill sound and the sound of air in the blood vessels). Diagnosis is made by exclusion. The differential diagnosis must be made with amniotic fluid embolus and the other cerebro-vascular accidents, as well as obstetrical shock. The principal factors that bring about air embolus are the entry of air into the dilated uterine veins which is helped by the negative pressure achieved by the Trendelenburg position. As soon as this diagnosis is made it is important to start hyperbaric oxygen treatment and symptomatic resuscitation.
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PMID:[Air embolus after Caesarean section (author's transl)]. 725 91

The clinical, physiologic, and pathologic manifestations of patent ductus arteriosus (PDA) with pulmonary hypertension (right to left type PDA) were studied in 5 dogs. Cyanosis, hindlimb collapse, low-intensity heart murmurs, and splitting of the 2nd heart sound were prominent clinical findings. Secondary polycythemia was a feature in 3 dogs. Electrocardiography revealed marked frontal plane right axis deviation in all dogs. Radiographic findings in all dogs consisted of an enlarged right ventricle and main pulmonary artery segment, with a hypovascular pulmonary pattern. A wide descending aorta was evident in 4 dogs. Pulmonary arteriography revealed blunt, tortuous secondary and tertiary vessels. Blood flow through the PDA was from right to left in 4 dogs and bidirectional in 1. Necropsy of 1 dog revealed extensive pulmonary arterial disease characterized by fibromuscular intimal proliferation. Surgical correction was contraindicated, and medical therapy was not required in the 4 dogs retained by the owners as pets. Due to the persisting congenital heart defect and the real and potential sequelae, the prognosis is guarded.
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PMID:Patent ductus arteriosus with pulmonary hypertension in the dog. 726 61

Five out of 6 foals between 2 and 4 months old, on a ranch in northern California, developed pneumonia within a 3 week period in June and July 1978. Corynebacterium equi was recovered from each of the 5 foals by transtracheal aspiration. Clinical signs were variable but included increased respiratory rate, fever, cough, nasal discharge, harsh airway sounds over middle sized airways and wheezing over small airways. Cyanosis was present in the most severely affected foal. Radiographic findings included diffusely increased interstitial and peribronchial densities, areas of consolidation and, in 3 cases, dense focal areas indicating abscessation. Foals were treated with several different antimicrobial agents. Most were treated with penicillin and gentamicin. Four of the 5 affected foals recovered within 2 to 3 weeks but the first foal to be affected died 2 days after first receiving veterinary attention. At postmortem examination, pulmonary changes considered typical of C equi pneumonia were found, including wet, heavy dark red lungs which failed to collapse and numerous 1 to 7 cm thin-walled abscesses throughout the parenchyma, containing inspissated exudate. C equi was cultured from the exudate. Samples of soil and dust from 9 of 20 areas inhabited by infected foals yielded C equi of the same serological group as found in the foals. Eight paddocks in which foals had not been kept were negative for C equi. The organism was recovered from cobwebs in the stalls occupied by infected foals. Aerosol infection via dust was considered to be the route of infection. Pharyngeal, vaginal and faecal cultures from the dams of 3 affected foals were negative for C equi. Early diagnosis by transtracheal aspiration and appropriate therapy are considered to be extremely important in the successful treatment of C equi pneumonia. Preventive therapy should include control of environmental dust.
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PMID:Studies of an outbreak of Corynebacterium equi pneumonia in foals. 731

This article reports a case of acute pancreatitis in a patient taking the oral contraceptive pill. A 32 year old mother had been on combined contraceptive pills since 1975. In 1978 she started having upper abdominal and retrosternal pain. She became critically ill with peripheral circulatory collapse, dyspnoea and cyanosis. A superficial thrombophlebitis was noted on the medial aspect of the right thigh. The diagnosis of pancreatitis was considered with history of recurrent abdominal pain. After several tests and supportive therapy (intravenous fluids, antibiotics, steriods), the woman started showing improvements in 48 hours and recovered in 10 days. This case differs from previously described cases in that the cholesterol and triglyceride levels were normal. The hypoglycemia has not been described previously.
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PMID:Contraceptive pills and acute pancreatitis. 732 5


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